A portent of catastrophic carbon dioxide embolism in laparoscopic hepatectomy: A case report

Introduction: Laparoscopic hepatectomy (LH) poses a high risk of carbon dioxide embolism due to extensive hepatic transection, long surgery duration, and dissection of the large hepatic veins or vena cava. Patient concerns: A 65-year-old man was scheduled to undergo LH. Following intraperitoneal carbon dioxide (CO2) insufflation and hepatic portal occlusion, the patient developed severe hemodynamic collapse accompanied by a decrease in the pulse oxygen saturation (SpO2). Diagnosis: Although a decrease in end-tidal carbon dioxide (ETCO2) was not observed, CO2 embolism was still suspected because of the symptoms. Interventions and Outcomes: The patient was successfully resuscitated after the immediate discontinuation of CO2 insufflation and inotrope administration. CO2 embolism must always be suspected during laparoscopic surgery whenever sudden hemodynamic collapse associated with decreased pulse oxygen saturation occurs, regardless of whether ETCO2 changes. Instant arterial blood gas analysis is imperative, and a significant difference between PaCO2 and ETCO2 is indicative of carbon dioxide embolism. Conclusion: Instant arterial blood gas analysis is imperative, and a significant difference between PaCO2 and ETCO2 is indicative of carbon dioxide embolism.


Introduction
Laparoscopic hepatectomy (LH) is an increasingly popular surgical treatment option for patients with liver disease.Despite the many advantages of LH, it is a well-known complication of CO 2 embolism.This complication, which is associated with a high mortality rate of approximately 28%, [1] may result in blockage of blood flow through the right ventricle (RV) or pulmonary artery, which may further result in heart failure. [2]LH poses a high risk of CO 2 embolism due to extensive hepatic transection, long duration of the surgery, and dissection of the large hepatic veins or vena cava.
End-tidal carbon dioxide (ETCO 2 ) monitoring has been suggested as a sensitive and non-invasive tool to monitor CO 2 embolism; most reports show that a significant decrease in ETCO 2 suggests CO 2 embolism. [3]In most studies, a marked decrease in ETCO2 suggests CO 2 embolism, but some literature states that in CO 2 embolization the drop in ETCO2 may be slight and transient or the ETCO2 drop may not be observed. [4]e report the case of a patient who suffered CO 2 embolism without decreased ETCO 2 during LH.The patient survived after immediate desufflation, ventilation with 100% oxygen, hyperventilation, and inotropic support.

Case presentation
The patient was a 65-year-old man with a body mass index of 21 kg/m 2 and American Society of Anesthesiologists physical SZ and XK contributed equally to this work.
The patient provided written informed consent for publication.The patient was scheduled for surgery and transferred to the operating room.Preoxygenation and monitoring were performed, which showed a BP of 180/70 mmHg, HR of 65 bpm, and pulse oxygen saturation (SPO 2 ) 100%.Considering his hypertension, 15 mg urapidil was administered instantly and dexmedetomidine (0.5µg/kg/h) was maintained for 40 minutes intravenously.Both the radial artery and internal jugular vein were cannulated under ultrasonic guidance to provide continuous monitoring of the arterial BP and central venous pressure, respectively.The BP decreased to 160/70 mm Hg 15 minutes later, after which general anesthesia was induced with 0.5 mg atropine, 12, 50, and 10 mg of etomidate, sufentanil, and cisatracurium, respectively.After tracheal intubation, continued mechanical ventilation of the lungs was initiated using a carbon dioxide absorption anesthetic breathing system.Anesthesia was maintained with continuous administration of propofol (4-10 mg/kg/h), remifentanil (0.1-0.2 µg/kg/min) and cisatracurium (0.1 mg/kg/h).The patient was then placed in a head-up and left-lateral position, and the operation was started.
Approximately 20 minutes later, the patient's BP gradually declined to 80/50 mm Hg after blocking the hepatic portal.The pneumoperitoneal pressure was 12 mm Hg, and the CVP was 5 cmH 2 O, with bleeding of 200 ml, urine output of 160 ml, and infusion of approximately 2000 ml.Ephedrine (6 mg) was administered intravenously to improve BP.Because of unstable BP, ephedrine (6 mg) was administered again.However, approximately 15 minutes later, severe hypotension abruptly manifested with a decrease in BP from 120/70 mm Hg to 75/50 mm Hg.The decrease in BP was also accompanied by hypoxemia, involving a decrease in SpO 2 from 100% to 85%.As the ETCO 2 was in the range of 36 to 43 mm Hg, the resident did not initially consider pulmonary embolism initially.In order to maintain hemodynamic stability, adrenaline (100µg) was administered repeatedly and phenylephrine (0.1-2 µg/kg/min) was also continuously infused.
Instant arterial blood gas analysis was performed simultaneously, which showed the following levels (the fraction of inspired oxygen was 60%): pH 7.07, PaCO 2 101 mm Hg, and PaO 2 77 mm Hg.Combining all the clues, the most probable reason for hemodynamic collapse and hypoxemia in this case was CO 2 embolism.We had taken a number of measures, including stopping surgical insufflation, adopting ventilation with 100% oxygen, hyperventilation, increasing positive end-expiratory pressure, infusing epinephrine and phenylephrine, and speeding up infusion.Systemic BP was maintained above 100 mm Hg with inotrope support, and 100% oxygen was administered, although systemic BP dropped from 110 mmHg to 80 mm Hg for several minutes.
After 10 minutes, a stable hemodynamic condition was achieved; the BP was in the range of 90/50 mm Hg to 150/90 mm Hg.In addition, SpO 2 was 100% again.A total of 100 µg epinephrine was administered, and approximately 3 mg phenylephrine was continuously infused, and the infusion was further accelerated thereafter.The surgery lasted for 135 minutes, with a total infusion volume of 3500 ml, bleeding volume of 400 ml, and urine output of 450 ml.Before leaving the operating room, atrial blood gas analysis was performed again, which showed a pH of 7.32, PaCO 2 46.5 mm Hg, and PaO 2 162 mm Hg.The patient was transferred to the post-anesthesia care unit (PACU) for further observation.As his condition improved and vital signs remained stable, the patient was extubated in the PACU without any complications.

Discussion
In recent years, LH has been regarded as an effective and safe surgical procedure for liver disease in select patients.However, laparoscopic surgery could result in CO 2 embolism. [5]Additionally, the unique hepatic anatomy, which has numerous large veins and the vena cava, can allow gas to enter into the circulatory system through high-pressure insufflation if vessel injuries occur during dissection of the extensive liver parenchyma. [6]As large gas emboli resulting in serious complications during laparoscopic liver biopsy are reported to occur in only 0.0016% of cases, anesthetists and surgeons might have underestimated the incidence of CO 2 embolism before. [7]Kim et al [8] reported the incidence of CO 2 embolism during total LH using transesophageal echocardiography (TEE) and stated that gas embolism was observed in all patients.
CO 2 emboli can obstruct the right chamber of the heart and pulmonary artery, which is a potentially fatal complication of anesthesia administered during laparoscopic surgery.The meaningful phenomena of gas embolism include decreased ETCO 2 , hypoxemia, hypercapnia, high airway pressure, and hemodynamic changes.In this case, the initial presentation was hypotension and hypoxia without decreased ETCO 2 .Therefore, we suspected other diseases such as hemorrhage, heart failure, and pneumothorax.Hepatic portal occlusions can also cause hypotension.However, the estimated blood loss was 200 ml, with 160 ml urine output and 2000 ml fluid infusion.Moreover, instant auscultation confirmed the presence of bilateral breath sounds.Considering the symptoms of hypoxia, rapid arterial blood analysis was performed.The diagnosis of CO 2 embolism was confirmed on the basis of the significant difference between PaCO 2 and ETCO 2.
This case demonstrates that severe hypotension accompanied by hypoxemia may indicate CO 2 embolism during laparoscopic surgery, regardless of ETCO 2 decreases.Unlike air or oxygen, CO 2 is more soluble in blood.Therefore, the clinical impact of CO 2 embolism during laparoscopy might be limited, and acute hypoxemia is rare.In addition, the pneumoperitoneum interferes with the potential hemodynamic effects due to CO 2 embolism, complicating the clinical diagnosis. [9]ETCO 2 monitoring is not very specific, and it may increase initially. [10]Moreover, the changes in ETCO 2 are rapid and sometimes of short duration; they could easily be missed in the operating theater. [11]urgeons should be informed immediately and stop insufflation when there is clinical suspicion of CO 2 embolism. [12]entilation with 100% oxygen could be used to wash out CO 2 and reduce ventilation-perfusion mismatch and hypoxemia. [13]Hyperventilation is also used to help eliminate CO 2 .Additionally, supportive treatment with fluids, vasopressors, and cardiopulmonary bypass may be necessary for patients with severe cardiovascular collapse. [8]Meanwhile, instant arterial blood analysis is especially important, which helps to diagnose the significant difference between PaCO 2 and ETCO 2 .
Besides ETCO 2 monitoring, TEE is the most sensitive method to detect CO 2 embolization compared with ETCO 2 and mean pulmonary artery pressure changes. [14]TEE can detect intravenous injection of CO 2 as small as 0.02 ml/kg. [15]However, the process of CO 2 embolism usually progresses rapidly.Thus, knowledge of the clinical symptoms of CO 2 embolism is much more practical.Furthermore, a central venous pressure line should be inserted in cardiac patients or in hemodynamically unstable patients, not only for hemodynamic monitoring but also as a way of attempting to remove gas emboli from the right atrium whenever gas embolization is suspected. [16]

Conclusion
This case shows that severe hypotension and hypoxemia under general anesthesia may indicate carbon dioxide embolism, although ETCO 2 does not decrease.Instant arterial The authors have no funding and conflicts of interest to disclose.